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Neural mechanisms and pathways involved in fuel restriction-induced changes in estrous behavior in Syrian hamsters
Abstract
Food availability is one of the most important environmental variables in controlling reproduction in mammals including humans. Undernutrition causes a delay of puberty, irregular menstrual/estrous cyclicity, and an impairment of sexual behavior. In female Syrian hamsters, food deprivation or treatment with metabolic inhibitors (2-deoxy- scD-glucose (2DG) and methyl palmoxirate (MP)) during estrous cycle days 1 and 2 suppresses the proestrous luteinizing hormone (LH) surge, blocks ovulation rate and inhibits lordosis. Taken together, this suggests that 48 h of fuel restriction cause a deficit in various aspects of reproduction function in Syrian hamsters. This dissertation investigated the possible neural mechanisms and neural pathways associated with fuel restriction-induced suppression of estrous behavior in Syrian hamsters. In the first experiment, 48 h of food deprivation or treatment with 2DG and MP inhibited steroid-induced lordosis in ovariectomized hamsters. However, neither 2DG nor MP given alone affected lordosis duration. To test the hypothesis that fuel restriction results in altered estradiol binding in the brain, immunocytochemistry for estrogen-receptor immunoreactivity (ERIR) was developed for hamster brain. Dense populations of ERIR cells were observed in the preoptic area, bed nucleus of stria terminalis, mediobasal hypothalamus, and amygdala. In the third experiment, fuel restriction for 48 h decreased the number of detectable ERIR cells in the ventromedial/ventrolateral hypothalamus (VMH/VLH), increased ERIR in the medial preoptic area (mPOA), but did not change ERIR in the nucleus of the solitary tract. The final experiment was designed to explore the possible neural relay loci in transmitting metabolic fuel information into the VMH/VMH and mPOA. The results showed that the area postrema, but not the vagus nerves, is required for the VMH/VLH to detect fuel availability. However, the vagus nerves, but not the area postrema, are required for the mPOA to detect fuel information. These results suggest that fuel restriction-induced suppression of lordosis is partially due to an alteration of estradiol binding in the brain and the level of VMH/VLH ERIR is correlated with the expression of lordosis. Furthermore, caudal hindbrain and the vagus nerves play an essential role for the transmission of metabolic fuel information to the ERIR cells in the VMH/VLH and mPOA, respectively.
Subject Area
Neurosciences
Recommended Citation
Li, Hui-Yun, "Neural mechanisms and pathways involved in fuel restriction-induced changes in estrous behavior in Syrian hamsters" (1994). Doctoral Dissertations Available from Proquest. AAI9420652.
https://scholarworks.umass.edu/dissertations/AAI9420652